Abstract

Background: A major cellular change in dopaminergic neurons leading to Parkinsonism is the alteration of microtubule proteins that causes accumulation of tau protein, α-syn and β-amyloid plaque in the cells. In this study we investigate the role of Vitamin D3 in relieving the symptoms of Parkinsonism as it is capable of stimulating polymerization of microtubules. The Microtubules (MT) system in the fish scale melanocytes has been modeled for the dopaminergic neurons of the Substantia Nigra (SN). These cells are capable of forming cellular processes similar to what is seen in the dopaminergic neurons; in this study, we investigate the protective effect of Vitamin D3 Receptor Agonist (VDRA) and N-Methyl-D-Aspartate Receptor (NMDA R) inhibition in process formation, synaptic denervation and melanin loss in fish scale melanocytes modeled as pigmented adrenergic cells. Method: The Tilapia scale was isolated and sub cultured in Ringer’s solution following which the cells were prepared for imaging. We incubated the cells with VDRA, Ketamine and a combination of Ketamine and VDRA in separate set ups for 60 minutes. Using brightfield imaging techniques, the cells were viewed during the incubation period and recorded using a Cameroscope connected to a computer interface. Results/Conclusion: The cells incubated with VDRA and NMDA R inhibitor, showed an increase in the number of process and extent of the process formation; the increased number of process is an indication of a rapid rate of polymerization of microtubules. Also, the processes formed are combined long processes peculiar to the NMDA R1 inhibition and short processes characteristic of VDR potentiation as seen in VDRA treatment only. Most of the effects of the VDRA were restricted to process formation around the cell body; this is similar to the microtubule cytoskeletal system found in the dendritic nucleation assembly. This finding confirms the presence of VDR and its likely restriction to d cell body plus its role in facilitating short dendrite-like process formation while NMDA R is located on the processes and facilitates long process formation.

Highlights

  • Selective vulnerability of the dopaminergic neurons and pigment cells of the Substantia Nigra (SN) cannot be over emphasized in the etiology and progression of PD

  • Most of the effects of the Vitamin D3 Receptor Agonist (VDRA) were restricted to process formation around the cell body; this is similar to the microtubule cytoskeletal system found in the dendritic nucleation assembly

  • Most of the effect of the VDRA was restricted to process formation around the cell body; this is similar to the microtubule cytoskeletal system found in the dendritic nucleation assembly of neurons

Read more

Summary

Introduction

The mechanism of the VDRA involves calcium signaling pathways that facilitate polymerization of MT such that the αβ-tubulin sub-units assemble and convey melanosomes and other vesicles to the periphery of the cell using the kinesin motor assembly [6] This is believed to be complimentary to the inhibition of NMDA R; prevention of glutamate toxicity [7], as such movement of vesicles, away from the nucleus prevents cell death by autophagy. The Microtubules (MT) system in the fish scale melanocytes has been modeled for the dopaminergic neurons of the Substantia Nigra (SN) These cells are capable of forming cellular processes similar to what is seen in the dopaminergic neurons; in this study, we investigate the protective effect of Vitamin D3 Receptor Agonist (VDRA) and N-Methyl-D-Aspartate Receptor (NMDA R) inhibition in process formation, synaptic denervation and melanin loss in fish scale melanocytes modeled as pigmented adrenergic cells

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call